Clinical Hyperbaric Oxygenation with Severe Oxygen Toxicity

Fuson, Robert L.; Saltzman, Herbert A.; Smith, Wirt W.; Whalen, Robert E.; Osterhout, Suydam; Parker, Roy T.

doi:10.1056/nejm196508192730803

Cited by 37 publications

(7 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…They were similar to those reported by Cederberg, Hallsten, and Miorner (1965). Almost precisely similar results were noted in the case reported by Fuson, Saltzman, Smith, Whalen, Osterhout, and Parker (1965) where a girl of 17 years of age was treated by hyperbaric oxygen at a concentration of 100I% at pressures up to 3 atmospheres. Death occurred after five days and here again pulmonary congestion, intraalveolar haemorrhage and hyaline membrane formation were in evidence.…”

Section: Oxygen At Atmospheric Pressuresupporting

confidence: 85%

The effect of oxygen on the lung

Claireaux¹

1975

J Clin Pathol

View full text Add to dashboard Cite

The harmful effect of oxygen in high concentration on the lung has been recognized for many years. Smith (1899) observed the lethal results following the exposure of experimental animals to oxygen at between 3 and 5 atmospheres pressure over a period of 24 hours. He considered that death resulted from pulmonary inflammation. Karsner (1916) and Binger, Faulkner, and Moore (1927) described widespread changes in the lungs of animals exposed to high concentrations of oxygen for 48 hours or more.

show abstract

Section: Oxygen At Atmospheric Pressuresupporting

confidence: 85%

The effect of oxygen on the lung

Claireaux¹

1975

J Clin Pathol

View full text Add to dashboard Cite

show abstract

“…Exposure of normal humans to oxygen at elevated pressure (that is, greater than 1 ATA O 2 ) has indicated a shorter duration of exposure for equivalent pulmonary symptoms and function changes (8,10,16,18). Pulmonary-related death has been reported for one patient in the normobaric O 2 exposure group (12) and another with hyperbaric exposure (9). Thus evidence of lung abnormalities with severity proportional to the partial pressure of oxygen has been demonstrated in normal human lungs similar to the findings with experimental animals.…”

mentioning

confidence: 54%

Hyperoxia and acute lung injury

Fisher¹,

Beers²

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

TO THE EDITOR: The review by has misleading and potentially dangerous statements concerning the role of hyperoxia in human acute lung injury (ALI). Table 4 states "in normal human lungs, 100% oxygen has not induced lung injury . . . " The text states that most mammalian species develop respiratory distress and die with exposure to 100% oxygen, but the "same findings have not been reproduced in humans with normal lungs . . . " That statement is essentially true (fortunately) but mainly because very few studies of potentially lethal hyperoxia have been carried out in individuals with normal lungs, for obvious reasons. The one study referenced in the review (1) was carried out in patients with irreversible brain injury, which may have influenced the pulmonary response to hyperoxia, and indeed a subsequent similar study demonstrated significant lung injury (13). Studies of normal individuals exposed experimentally to 100% oxygen at normal pressure (i.e., 1 ATA) have shown evidence of tracheobronchitis and changes in vital capacity, diffusing capacity, and lung permeability (2-5, 7, 17). Inadvertent exposure of patients with normal lungs to prolonged hyperoxia resulted in clinical findings compatible with oxygen toxicity (12). Exposure of normal humans to oxygen at elevated pressure (that is, greater than 1 ATA O 2 ) has indicated a shorter duration of exposure for equivalent pulmonary symptoms and function changes (8,10,16,18). Pulmonary-related death has been reported for one patient in the normobaric O 2 exposure group (12) and another with hyperbaric exposure (9). Thus evidence of lung abnormalities with severity proportional to the partial pressure of oxygen has been demonstrated in normal human lungs similar to the findings with experimental animals. It is known that different species, and indeed strains of the same species as well as individuals from the same strain, show varying sensitivity to the toxic effects of oxygen (11). Rats exposed to 0.8 ATA O 2 become tolerant to 1 ATA O 2 but uniformly die when subsequently exposed to higher (1.5 ATA) O 2 partial pressures (14), emphasizing the importance of O 2 "dose." Parenthetically, the dose range for lethality (approximately 0.8 -1.5 ATA) is quite narrow compared with many toxicants where dose sensitivity of various species may vary by more than an order of magnitude. So the important question is, what is the dose range for human pulmonary oxygen toxicity? Based on the limited number of human studies but with analogy to nonhuman primates (6), the "average" human might require O 2 at 1.1 or 1.2 ATA to reach a lethal concentration. If that is the case, a large segment of the human population might be spared ALI and lethality with 100% oxygen at 1 ATA. However, that concentration of oxygen could prove to be lethal for that fraction of the population whose resistance to oxidant stress is less than the population mean. All indications are that hyperoxia in animals (with appropriate consideration of dose) does serve as a model for human ALI associated with oxidant...

show abstract

“…The present study was undertaken to elucidate the nature and time-course of damage occurring in the lungs of rats breathing essentially pure oxygen at atmospheric pressure. Previous studies (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) had shown that disturbances in the alveolar space and capillary bed (25) were associated with damages, in lung tissues, which comprise accumulation of edema fluid and cells in the interstitial space, a thickening of the air-blood barrier, and changes in the fine structure of cells (26)(27)(28). While these findings, for the most part, were recorded in terminal phases of oxygen poisoning, the present study attempts to define the time-course of events from their inception to their final stages, by apply-ing methods of quantitative morphology and electron microscopy to a time series of oxygen exposure experiments.…”

Section: Introductionmentioning

confidence: 99%

Development of Fine Structural Damage to Alveolar and Capillary Lining Cells in Oxygen-Poisoned Rat Lungs

Kistler

Caldwell

Weibel

1967

The Journal of Cell Biology

347

View full text Add to dashboard Cite

Rats were exposed to 98.5% oxygen at 765 torr for 6-72 hr. The pulmonary changes were investigatcd by electron microscopy and by morphomctric methods. A progressive thickcning of thc air-blood barrier, from the normal 1.5 to 3 # after 3 days, was duc primarily to enlargement of thc interstitial space by accumulation of edema which was replaced secondarily by cells and fibrin. This was accompanicd by destruction of about 50% of the capillaries. Morphomctric data allowed an cstimatc of the degree of impairment of lung function. The primary cellular damagc was located in endothelial cells which underwent cytoplasmic changes and, finally, fragmentation. In contrast, thc damage to the epithelial lining of alvcoli was relatively scarce compared to thc extcnsivc cndothclial changes. This pertained cven to severely damaged lungs with 65 % of the alveoli obliterated by a heterogeneous cxudatc. Possiblc causes for this apparently different reaction of epithelium (thc first target ccll) and cndothelium to toxic oxygen cffccts are discussed.

show abstract

Clinical Hyperbaric Oxygenation with Severe Oxygen Toxicity

Cited by 37 publications

References 5 publications

The effect of oxygen on the lung

The effect of oxygen on the lung

Hyperoxia and acute lung injury

Development of Fine Structural Damage to Alveolar and Capillary Lining Cells in Oxygen-Poisoned Rat Lungs

Contact Info

Product

Resources

About